These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Interleukin 17A in atherosclerosis - Regulation and pathophysiologic effector function.
    Author: Nordlohne J, von Vietinghoff S.
    Journal: Cytokine; 2019 Oct; 122():154089. PubMed ID: 28663097.
    Abstract:
    This review summarizes the current data on the interleukin (IL)-17A pathway in experimental atherosclerosis and clinical data. IL-17A is a prominent cytokine for early T cell response produced by both innate and adaptive leukocytes. In atherosclerosis, increased total IL-17A levels and expression in CD4+ T helper and γδ T cells have been demonstrated. Cytokines including IL-6 and TGFβ that increase IL-17A expression are elevated. Many other factors such as lipids, glucose and sodium chloride concentrations as well as vitamins and arylhydrocarbon receptor agonists that promote IL-17A expression are closely associated with cardiovascular risk in the human population. In acute inflammation models, IL-17A mediates innate leukocyte recruitment of both neutrophils and monocytes. In atherosclerosis, IL-17A increased aortic macrophage and T cell infiltration in most models. Secondary recruitment effects via the endothelium and according to recent data also pericytes have been demonstrated. IL-17 receptor A is highly expressed on monocytes and direct effects have been reported as well. Beyond leukocyte accumulation, IL-17A may affect other factors of plaque formation such as endothelial function, and according to some reports, fibrous cap formation and vascular relaxation with an increase in blood pressure. Anti-IL-17A agents are now available for clinical use. Cardiovascular side effect profiles are benign at this point. IL-17A appears to be a differential regulator of atherosclerosis and its effects in mouse models suggest that its modulation may have contradictory effects on plaque size and possibly stability in different patient populations.
    [Abstract] [Full Text] [Related] [New Search]